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A
You go to McDonald's, that is a metabolic toxin. You are actively poisoning yourself. If you have been eating McDonald's and lots of seed oils your whole life, if you stop today, it takes you potentially four plus years to fully recycle the membranes of all the cells in your body.
B
I think that people don't realize all the places that they're hidden.
A
I'm there everywhere.
B
Potato chips, nearly every dressing that you pull off of the shelf in breads.
A
There are so many markers of inflammation that increase when you fill the body with these oxidation prone oils. And yet the mainstream perspective, Harvard, many apparently intelligent physicians in the community, longevity influencers, are still holding fast to the claim that seed oils are benign for humans. And I would argue that the best trials with seed oils clearly show they're harmful. It's just that these trials have been suppressed.
B
And you know what I find is that a lot of randomized clinical trials essentially end up proving what we know ancestrally from nature. It always takes us back to the basics.
A
You can't go wrong eating simple whole foods. It's just unprocessed animal foods, unprocessed plant foods. You'll be great.
B
We take the narrative that these seed oils are bad for you. So I think we just need to put it into context. Why are we attacking this plant? Why are we in the oil extraction method?
A
The only thing that seed oils might have going for them is a.
B
Ultimate human. Hey, guys, welcome back to the ultimate human podcast. You know the drill. I'm your host, Gary Brea, human biologist, where we go down the road of everything. Anti aging, biohacking, longevity, and everything in between. One of my favorite house guests has paid me a visit again before Thanksgiving. And even though he didn't know it, let's go. I'm like, every time we meet in the kitchen, you know, we, we, we start running a podcast together. And I was like, dude, let's just go in the studio and, and rip this because this is really, really good content. Welcome back to the show, Paul Saladino.
A
It's always good to see you, man. I'm happy to do it.
B
Yeah. So Dr. Paul Saladino and I have formed an unbelievable friendship, you know, over the last few years. Not just being in the same industry, but spending a lot of time in close proximity and really practices what he preaches, that I practice what I preach. And you know, every time we meet in the morning, you know, he, I, I caught him this morning getting his sunlight and doing stretches outside on the balcony in the sun. I was like, hey, I'm I'm getting ready to go out there and do my breath work myself. And he comes back in, he goes, let me show you my morning elixir. He starts breaking open these capsules of testicle and, and, and B vitamins and honey. And you know, we've had raw colostrum over the last few days. I feel amazing. And we just started going back and forth about a recent documentary that he published, which is phenomenal. I'm going to put the link in the show notes below. You've got to watch this documentary, which I think finally closes the chapter on seed oils and the inflammatory nature of these oils and their implications in many of the chronic disease conditions that we are blaming on other natural compounds in the body like cholesterol. And that is not to say that we shouldn't keep an eye on cholesterol. But my point is that we have been, we have been blaming the firemen for the fire for too many years. And the notion that if we had less firemen, we'd have fewer fires is simply a fallacy. And the, the, the large data is starting to prove that. So Paul, I, I would love it if you would just give us a little background on the documentary, like what led to it and give us, give us an overview of what, what we're going to see in the documentary. And I specifically want to go down in detail the road of seed oils because just yesterday one of the biggest, you know, gurus, longevity gurus in our space, we just talked about, I won't name any names, you know, posted that, that seed oils were safe.
A
It's crazy. So this is a mini documentary. It's only about 37 minutes long. And I did it in collaboration with heart and soil supplements. So those testicle pills that I was emptying into your raw milk this morning.
B
They'Re actually pretty good. I mean, we put, we put it in raw milk and then we added honey.
A
Honey? Yeah, you can't even taste them too.
B
So good.
A
Those are testicle pills from Hard and Soil supplements. And Hard and Soil is just a company that I built tell people get organs in the capsules. But Hardened Soil has an amazing research team and I collaborated with them to make this mini documentary on seed oils. It's called Fed a Lie. And it's a, it's kind of an entry level seed oil documentary. It's just to get people asking the questions. So I'm in the documentary. Chris Kenobi is in the documentary. He's an md, he's an ophthalmologist, and Nina Teicholtz is in the documentary who wrote a Big Fat Big Fat Surprise.
B
The Big Fat Surprise, yeah.
A
Detailing a lot of the sort of corruption and confusion in the space around the history around saturated fat versus.
B
You're not saying that there's corruption in.
A
Our nutritional food industry. Imagine that. Perhaps a little bit of corruption. We can talk about it. But what's so interesting when you think about this from the perspective of seed oils and the history is that we really have been, I believe, fed a lie regarding their benign nature or their health benefits. And as you suggested, it kind of all centers around this idea of cholesterol. So the only thing that seed oils might have going for them is that they lower apob. They lower your cholesterol, quote, unquote.
B
Yeah.
A
And the mainstream medical paradigm, which I was trained in, perhaps propagandized.
B
He's a medical doctor, by the way. He is an md.
A
Yeah. Is. Is all about lowering cholesterol, often in a myopic view. Right. So if you are an md, you are basically trained to lower APOB and or LDL cholesterol no matter what, without much attention to other metrics that may have more weight on your cardiovascular risk or that are simply more relevant, like oxidized LDL, Lp, Lppla2, which is lipoprotein associated phospholipase A2. And this is where it starts to get interesting because I'll say this about seed oils. I think you could come to the conclusion that seed oils are benign for humans if you ignore all historical data, all evolutionary precedent. Humans have never had this in our diets. You ignore all animal studies which clearly show that seed oils increase rates of cancer, non alcoholic steato hepatitis, which is liver injury. That's very bad in animals. They increase adiposity, they increase cardiovascular disease in animal models. You have to ignore all mechanistic studies which clearly show that linoleic acid, this 18 carbon omega 6 fatty acid, is very susceptible to oxidation in. In biological systems. And you also have to kind of cherry pick the randomized controlled trials in humans and ignore the randomized control trials in humans that show that when you feed people seed oils versus olive oil or saturated fat, they have increased oxidized LDL, increase LP and increased LPP increase LP, increased LP 7 to 10%.
B
Yeah, and that's usually a genetic. More of a genetic predisposition. I actually, I actually have high lp. My cholesterol levels are great and I'm very cautious about what I eat. So I take bergamot O, I take slow release niacin that's, that's helped. I've done tpe, Total plasma exchange. That really helped.
A
We can talk about lp because I, I want to share with you some data from my friend Dave Feldman about LP also.
B
Really?
A
Yeah, we'll get very interested in that.
B
Because a lot of folks that are watching this, you know, that have.
A
They worry about lp.
B
What's interesting, but, you know, before we get on this road is, and we've talked about this before is, you know, in the mortality space, when we were doing mortality research tables, when we were building these probabilistic models, it was very apparent to us that the people that were living the, the longest all had, and I'm just picking one, you know, isolated portion of cholesterol, but they all had elevated levels of LDL cholesterol right at the time of their death. We would process a lot of death claims on, on folks that were, at the time they passed, they were in nursing homes and they actually, we did have, you know, blood work on them. And I don't recall a time, there may have been, but I don't recall a time where we processed a death claim on a centenarian, someone over the age of 100 that did not have clinically elevated levels of LDL cholesterol at the time of their death. And, and so we actually didn't use randomized clinical trials. We used big data. Right. But, but I want to, I want to get back to the seed oils and I want to sort of walk people through this because, because I think inherently people think sunflower good. Rapeseed. It's a plant good, you know, eaten by humans.
A
We can talk about rapesee.
B
Yeah, yeah, yeah. You know, and, and, and I know the whole, you know, evolution of industrial. But I'm just saying for, for, for the general public, I see soybean oil. Soybeans are healthy. I mean, sunflower oil. Sunflowers are great. I eat sunflower.
A
Right.
B
And so, so then we take the narrative that these seed oils are bad for you. So I think we just need to put it into context or, you know, why are we attacking this plant? Why are we attacking the oil extraction method?
A
Right. So seed oils are often called vegetable oils. And I think that's kind of a, A marketing claim. Right? That's a euphemism. They're, they're seed oils. They're called vegetable oils, probably because we all associate vegetables with health, which is a separate. Yeah, but in order to get oil out of a plant seed, whether it's a rape seed, which is the Precursor of canola oil or a soybean or a peanut or I mean, sunflower, corn. Right. Corn, corn, canola, sunflower, safflower, grapeseed, rice bran. All of these are seed oils. You have to do refining, bleaching and deodorization. And if anyone has ever seen a seed oil factory, it looks like an oil refinery because that's what it is. Yeah, there's huge smokestacks with, you know, either water condensation vapor coming out or other pollutants coming out of the smokestacks. It's a huge, huge process with grinding, with extraction, with de gumming, with deodorization. We've talked about this extraction with hexane contaminated hydroxide. Right.
B
Very often bleach.
A
Yeah, they're, they're refined, bleached and deodorized oils. And the heating process in seed oils, it starts with a grinding step, then they're heated to 200 degrees, then they're heated to like 300 degrees, and then they're heated to over 400, 500 degrees Fahrenheit. Remember, this is an omega 6 polyunsaturated fat rich oil. Sometimes up to 55 of the oil is linoleic acid. And when you heat linoleic acid to 500 degrees degrees Fahrenheit, you get massive amounts of lipid peroxides, which is essentially rusted oil or rancid oxidized oil. And it's just, this is the nature of the oil. This is organic chemistry. You cannot avoid this. So people have looked at levels of lipid peroxides. These are oxidized oils and these are reactive products. When you put these into your body, they initiate a chain reaction. And that chain reaction can partially be quelled or stopped by things like vitamin E or vitamin C, depending on what, whether you're in the lipid soluble or the water soluble fraction of your body. But it cannot entirely be be abolished like you're, this uses up resources in your body. And the idea with seed oils is that when you eat polyunsaturated fats, whether it's from fish oil or from seed oils, we store these and we talked about this last night in our pre four and a half years, essentially, yes, there is some interesting data about the kinetics of how we hold onto these oils and it's not easy for us to get rid of them. So when you are eating french fries cooked in seed oils, which are even more oxidized because it's been a fryer oil that hasn't been changed for a week, you know, I've been to McDonald's, I've been to KFC. And I ask them, how often do you change the fryer oil? Both of them, about every once a week. You know, you go to in and out, how often do you change the fryer oil? Once a week. Once a week you're frying 16, 20 hours a day in this oil that's very susceptible to oxidation. And if you're getting french fries cooked in seed oils that have been fried in that for a week, you are getting massively increased levels of these lipid peroxides. Not to even mention the fact that increasing polyunsaturated fats in the human diet evolutionarily is inconsistent. And we store all of these, it creates this oxidative stress burden in our bodies. It's just like having a bunch of dry wood stored at your cabin in the mountains in the middle of a lightning storm. This isn't a good idea. If you have a lot of dry wood in your body, the dry wood being the oxidation susceptible linoleic acid, and you have lots of sparks, you're going to get lots of fires and then you're going to overwhelm your body's resources and you can run into real problems. Now people always say seed oils are inflammatory and the counter argument is there's no evidence that seed oils are inflammatory because there are some studies which show that seed oils maybe don't increase canonical inflammatory markers like CRP. But I would argue that oxidized LDL, LP and LPPLA2 are clearly inflammatory markers. So this is just, this is just semantics, I think. Yeah.
B
Cherry picking the.
A
Yes.
B
Because it doesn't create a non specific marker of inflammation like C reactive protein. You're like, it's not driving inflammation. Well, that's not the only marker.
A
There are so many markers of inflammation and one of the things CRP does is bind oxidized ldl. Right. So the CRP and oxidized LDL are intimately linked. And so to say that there's no inflammatory markers with seed oils is ludicrous. It's just closing your eyes and putting your hands in your ears and saying la la la. You know, there's, I don't see any crp.
B
Yeah.
A
You know, just because ESR doesn't go up erythrocyte sedimentation rate with seed oils there are so many markers of inflammation that increases Right. When you, when you fill the body with these oxidation prone oils. And yet the mainstream perspective, Harvard Mayo, many apparently intelligent physicians in the community, longevity influencers are still holding fast to the claim that seed oils are benign for humans. And so we just wanted it with hardened soil. I just wanted to make a documentary that got people talking about this and at a higher level, asking questions about why we still think these are healthy. How anyone can even say that? Because when you look at the highest level of evidence, the randomized controlled trials with seed oils, and I, I have a whole thread on X that I did months ago about this and I just, I just resurfaced the tweet this morning. I broke down all 11 of the randomized controlled trials in humans with seed oils. Because that's the highest level of evidence. Right. You, I, I went through it earlier in this podcast. We talked about evolutionarily inconsistent. We've never had cereals in our diet. Mechanistic studies.
B
How do we.
A
Very bad.
B
How do we, how do we introduced seed oils? Because we've had polyunsaturated fatty acids. But I mean, in small amounts.
A
Yeah, right. You know, historically. Or nuts. Basically, small amounts of nuts. But how many almonds can you eat? You know, almonds are a recent addition to the human diet. They, you know, but sure, there are some hunter gatherers that have mongongo nuts like the koisan. But most of us, historically, throughout our evolution as humans, had very small amounts of polyunsaturated fats in our diets. And if you look at hunter gatherers or indigenous cultures, very small amounts, 1, 2% of their calories from polyunsaturated fats. Now we are eating 40 or, you know, 10 to 15 of our calories and then it increases even from there for us. So average Americans today eat five tablespoons of some combination of seed oils. Five tablespoons, that's hundreds of calories.
B
And I think that people don't realize all the places that they're hidden. I mean, everywhere. Potato chips in, in, in snack foods, in, in nearly every dressing that you pulled the shelf in.
A
Breads, breads have it. Like you said, dressings.
B
Yeah. And even some of the good dressings. And it'll, it'll say, you know, what about expeller pressed?
A
So when you have an expeller pressed oil, now, let's be honest, there's a very, very small fraction, probably less than a tenth of a percent of all seed oils are expeller pressed.
B
Right.
A
You don't have the refining, the bleaching and the deodorization. So that's a less oxidized oil, but you still have a very fragile oil that has been stripped from the seed matrix and is going to be susceptible to oxidation. It's less oxidized. But I still think it's an evolutionarily inappropriate thing to consume as a human because you're still stuffing your cells with these oxidation prone seed oils. And so if we get back to the randomized control trials, of these 11 trials. Right. The majority of them are flawed, fundamentally flawed, because they were done from the 1950s to the 1980s, and we didn't really have a good sense of trans fat in that time. Trans fat was really only banned from food in what, the late 18, 1980s or 1990s. So almost every single one of these trials has trans fats in the control group. And the control group in these randomized control trials is comparing saturated fat rich diets in the control group to polyunsaturated fat rich diets. So what do you think happens in a randomized controlled trial if the control group eating saturated fat has significantly more trans fats than the experimental group eating polyunsaturated fats? Right, that's a problem.
B
Yeah.
A
Right. And many of these trials are also multifactorial interventions. Things like, oh, in the control group we're going to say eat your normal diet, which is perhaps animal fat rich, but you're probably also eating margarine with trans fats because we didn't tell you to stop doing that. And the experimental group, we're going to say eat more seed oils, but also exercise more, eat more vegetables and stop smoking. And these are the type of randomized controlled trials that form the, quote, bedrock of the fact checkers. When I get fact check on Instagram or meta, any meta platform for saying that seed oils are harmful for humans, they'll say, no, there's a randomized controlled trial here, or there's a meta analysis here, or here's a an AFP fact check article where people have said seed oils are fine based on these foundationally fundamentally flawed randomized control trials. And the randomized control trials that show seed oils to be harmful are suppressed. Sydney Diet Heart, Minnesota coronary experiment at the Rose Corn oil trial was one of the first trials done on seed oils in the late 1950s. And it was underpowered, but it clearly showed that seed oils were very harmful for humans. A significantly higher amount of people in the seed oil group versus the saturated fat group had heart attacks. Wow. And the p value was between.05 and 0.1. So there was less than a one in a thousand chance that this result showing cedar oils are harmful happens by chance less than one in a thousand. But because the P value wasn't less than.0. Five people say it wasn't a significant finding that should have been case closed for seed oils in the 1950s.
B
Wow.
A
But there were still 10 more randomized control trials that many of which almost.
B
Funded by the food industry.
A
Funded by the food industry or which confuse the data, which are very complex trials. And there isn't a perfect trial done with seed oils. But I would argue that the best trials with cereals clearly show they're harmful. It's just that these trials have been suppressed. And as you know, with a meta analysis, a researcher like Darius Mozaffari and at Tufts who gifted us with the food compass system, which tells us that Fruit Loops and Cheerios are healthier than ground beef and eggs.
B
Yeah.
A
Can write a meta analysis on seed oils. And he's done this and he can leave out things like Sydney diet, heart. He can just choose which trials he wants to put in his meta analysis and write in the abstract that seed oils are benign or trend toward cardiovascular benefit for humans. This is ludicrous.
B
Wow.
A
This is ludicrous. This is, this is the state of the affairs right now.
B
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A
Wow.
B
And, and, and, and by third world, you know, these are people that don't have consistent access to sanitation, to, to sanitary, clean drinking water. They might not have consistent access to sanitary sewage systems. You know, removing the, you know, this, the waste and sewage from, from close proximity to where they live. But they also don't have a lot of access to highly processed foods, seed oils, you know, they're by default eating whole foods.
A
Right.
B
And it's astounding when you think some, someone living in a, in a first world nation like the United States that spends four and a half trillion dollars a year on health care is actually not outliving somebody that is essentially living outside under a tin roof, you know, bathing in a stream where the cows bathe and defecate. It's pretty, it says a lot about the state of affairs of where we are. So what are, what is the, so you have this oxidized oil, and I think you could probably make the same argument for burned meat, you know, nitrates, a lot of, a lot of other things that, that can happen when, you know, if you overcook things or over char things or. But, but you, you have this highly oxidized oil, it gets into the body and then what happens? I mean, I know we all know inflammation is bad, but what is it about the inflammation that is bad? What is it that is it doing to the endothelial lining of the artery? Or how is it creating this contact surface that is attracting cholesterol, which I think a lot of people don't realize that cholesterol is called to the site of inflammation. It's usually called to repair a tissue. It doesn't just magically just jump out of the bloodstream and stick, stick to the wall.
A
I don't think it doesn't do that.
B
No.
A
Native ldl. Native ldl, it's you, you would have a hard time arguing, looking at the medical literature, that native LDL that is unoxidized, unmodified LDL is atherogenic. Right. So something has to Happen to our LDL to make it participate either to.
B
The LDL or to the endothelial wall or both.
A
Probably the. I would argue the endothelial wall is the proximate event of atherosclerosis, because we know that. We know that really uninjured endothelium and uninjured arteries don't really accumulate ldl. So you can think about this, and we may have talked about this on a previous podcast, but if we're talking about LDL or apob containing lipoproteins, which is a slightly broader family than just ldl, we have. I have the same amount of LDL circulating in my veins. You know, you. You. You have veins on your arm, too. You can see that these are returning blood to my heart from my hands. Deeper in my arm, I have arteries that are pumping blood to my hands, and in between, there are capillaries. So I have a continuous system of blood flow. The last time I checked my cholesterol, which was about a month ago, my LDL, I think, was 125 milligrams per deciliter.
B
Okay.
A
My APOB is probably just over 100 or just below 100.
B
So a lot of physicians would consider that high. Above 99.
A
Yeah, somebody would consider it high.
B
Yeah.
A
I have the same amount of LDL circulating to my hands, moving through the capillaries, and coming back in my veins. But in me and all humans, we do not see atherosclerosis occurring in native veins. So atherosclerosis doesn't occur in a vein at all. In humans, it's because it's lower pressure. And when you have lower pressure in a vein, you don't denude the endothelium. You don't create proximate endothelial injury that is necessary to start atherosclerosis. If APOB containing lipoproteins, I.e. lDL, plus its cousins are atherogenic, why don't we get atherosclerosis and veins? They have the exact same endothelial lining on the inside. If you were in a little spaceship like Rick Moranis and, honey, I'm like, what is that? Like in, you know, inner space or whatever, you know, if you're running through my body in the artery and the vein, if I put you inside a vein or I put you inside an artery, and you're looking from the inside of the vessel to the wall, it looks the same. It looks the same. The inside of an artery and the inside of a vein are the same. The endothelium is the same, yeah.
B
It's just on the outside of the endothelium, you'll have smooth muscle versus.
A
Versus. Yeah, versus more musculine or more musculature and artery to help it contract.
B
Right.
A
And. And you can actually take a vein and you can transplant it into the arterial circulation. So we do this in coronary artery bypass grafting. You can take a vein, usually from the leg or, you know, other places in the body, and you can transplant it into the arterial circulation. So you can take a vein and put it in the arterial circulation and it actually gets atherosclerosis very quickly because it is subjected to higher pressure and that denudes the endothelium. So when a vein is in the arterial circulation and it has that sort of proximate event, that arterial inner endothelial damage, it will accumulate atherosclerosis, but it doesn't happen in native circulation. And I would argue that is a very strong argument that apob is not causal because I have the same amount of apob in my veins. If it's. If it's so bad for my arteries and, and my veins, you know, if it's so bad for my endothelium, why isn't it damaging the endothelium in my veins? Because it needs a proximate event to have that happen. Now circle back to humans today in 2024, there are many studies which suggest that 86 to 93% of us have at least one marker of metabolic dysfunction. Right. And these are the metabolic syndrome criteria. But I think if you look around our population today, which you were hinting at, it's pretty sad. Many of us are obese and many of us are on a continuum of insulin resistance.
B
Right.
A
And when you start to develop insulin resistance, and I'll talk about how this is probably related to seed oils in a moment, when you develop insulin resistance, I think this is what's impairing your immune system. We know that diabetics, full blown insulin resistance, have a lot of trouble regulating their immune system. They can get a cut on their toe and they can lose their foot. Right. Because they have such poor immune function. So as you move along this continuum of insulin resistance, the immune system suffers, and this is shown over and over and over, that insulin resistance impairs immune function. So I believe what's going on here is that in a diabetic, in any human that is on this pathway of insulin resistance, which we know is related to our processed foods and our lifestyle, you have impairment of the immune system in the arterial wall. So when you cut your knee, say you're like surfing or. And you hit a reef or you're skateboarding or you're dancing or whatever, you're playing baseball, and you skin your knee, your immune system goes there to repair the knee. Well, all of us are getting, quote, skin knees on the inside of our arteries because all of us have higher pressure in our arteries. But diabetics, anyone on this insulin resistance spectrum or continuum is going to have trouble repairing the endothelial damage that happens from daily life. And that, I think, is what's going on for diabetics that is causing atherosclerosis. All of us get damage to the arteries. Most of us can repair it. Just like we, you know. I was playing a pickleball in Phoenix recently. I was there to surf a wave pool. And I ran into a wall, right? I was going off the court because I stink a pickleball. And I. And I ran into a cement wall that was there. And I had. I had, like, I had a little. A little strawberry on my knee. I had a little skin on my knee. My immune system repairs it, right? But when you have insulin resistance, it doesn't get repaired in time. And I think that is where the atherosclerosis starts. Diabetics have continuous damage without functional, actual, true repair on the inside of their arteries. And that, I think, is what's going on that no one's talking about. So the problem is not ldl. We should pay attention to it if you're diabetic, okay, pay attention to it. But the problem is not the ldl. The problem is the insulin resistance and the immune dysfunction that comes with it, and the persistent damage to the endothelium, the persistent damage to arteries that comes with it, which leaves you susceptible, right? Going back to the wood analogy, we have ldl, and I'm mixing my metaphors here, but I think about LDL as wood. And wood doesn't cause a fire, right? Unless there's a spark, right? And you can build things out of wood. You can build a cabin out of wood. But when you have more sparks, hormones.
B
Yeah. Cell walls, cell membranes, vitamin D3.
A
It does all of these things.
B
Lots of things are made from clothes.
A
Yes. Sex, cell membranes. We need ldl. We need. LDL is the carrier. LDL is the carrier for all of these vital things in the human body. It doesn't initiate atherosclerosis, but if you have lots of sparks, that dry wood can light on fire. Right? And again, I'm mixing my metaphors here. I talked about pufa earlier as dry wood, but let's talk about LDL as drywood here.
B
Yeah.
A
So, yeah, hopefully that's not confusing for people. But you. I get the idea that, like, wood doesn't spontaneously combust into a fire. Right, right. Like wood is valuable. LDL is valuable in the human body. It also has immune roles. So to say that APOB is what we should be lowering without any attention to insulin sensitivity, oxidized LDL LP is just ludicrous to me. There's so much more to the picture here.
B
Yeah. We want to make it so simple that LDL high cardiovascular risk, high. LDL low cardiovascular risk, low. So all you have to do is hammer this down and, you know, it's, it's, it is astounding to me that most of the time we're actually not talking about, you know, the toxic soup that we're bathing our cellular biology and we want to, we want to continue to bathe our cellular biology in this toxic soup and then, and then come down on top of it with a chemical or a synthetic pharmaceutical and, and allow that to be the answer without actually changing the habitual pattern that brought you there. I mean, a lot of times when people talk to me about really wanting to lose weight, I walk them through, you know, for. Not to sound harsh, but why are you so fat? Right. Let's figure out why you're so heavy and then let's not do that. And in the process of doing that, we're also going to put some components in place to make sure that you, you really, you know, you, you lose weight quickly and safely and everything else. But to reframe the way that we talk about the state of, of the condition that we're in, you know, if you've got metabolic syndrome, the answer isn't, okay, well, let's add insulin and metformin and, and, you know, beta blocker, calcium channel blocker, diuretic, blood thinner is not to take the, the results of this toxic soup and start to manage it with synthetics and, and chemicals and pharmaceuticals. But it's to say, how do we get into this condition in the first place? And, you know, and I think, you know, as I became more and more aware of seed oils, I mean, I have to say, for the consumer, it's hard. I mean, it is, it is difficult to walk down a grocery store aisle. And, you know, the deception, in my opinion, in food labeling too, you know, heart healthy is right on the seed oil bottle. By the way, brother, I was in.
A
Costco the other day filming and the corn oil has a big heart. Healthy.
B
Yeah.
A
Label it.
B
It's got the little heart.
A
How is this possible? Right.
B
Emoji.
A
Because it look like this is, this is ludicrous. So let's talk about, let's talk about how we get insulin resistant and. Because this is interesting to me.
B
Yeah.
A
So when, when you go to your doctor and I want the people that are listening to think about this. And your doctor checks your cholesterol, how often does your doctor do any metric that approximates your insulin sensitivity? Right. They're not really telling you about fasting insulin. I have to constantly talk to people and say, ask your doctor for a fasting insulin. It's a thirty dollar test that your insurance should pay for. But maybe your insurance won't pay. But it's $30.
B
Right.
A
For the amount of information it gives you.
B
And most glucose, hemoglobin, A1C, all of those also.
A
Or ratios of triglycerides. Right. But I think fasting insulin is such a good metric of insulin sensitivity and no one is getting it. And, and you're interpreting lipids without any context of your insulin sensitivity. I think every lipid panel should be paired with insulin, fasting insulin, because your lipids matter in the context of your insulin sensitivity. And this goes back to Dave Feldman's research, which we will get to. But I think that what's happening here for people, and this is where it gets really interesting. And we don't have of randomized controlled trials here, so we're approximating mechanistic data. But it's really interesting to say that as we talked about earlier, when you eat polyunsaturated fats, they get stored in your body. We, we just are full of them. And you mentioned a number earlier that it's important to, to bring up again, which is the fact that looking at kinetic studies of how we accumulate fatty acids, most people estimate that if you have been eating McDonald's and lots of seed oils your whole life, it takes you potentially four plus years if you stop today to fully recycle the membranes of all the cells in your body. The fatty acid depots like the fat tissue probably being the least quick to recycle, but it probably takes about four years to, to really fully change the composition of all the cell membranes and all the mitochondrial membranes.
B
Wow.
A
That's a big deal. Right? There are potentially ways to speed that up that we can talk about, but they're, they're pretty intense.
B
Yeah, I'd like to talk about those.
A
Yeah. So. But what's going on is we are stuffing our cell membranes and we are stuffing our mitochondrial membranes with polyunsaturated fatty acids. Our bodies change based on what we're eating. This is the thing that, like, not all calories are created equally. The last time we talked, we talked about my, my, My frustration with the notion that you can just eat less calories and even eat bad food, that you can somehow out diet or out exercise, a bad diet. It's not true. Because if you are eating French fries, yes, you could lose weight eating french fries, but you are immediately stuffing all of your cell membranes, all of your mitochondrial membranes, all of the cells in your fatty acid depots with more polyunsaturated fatty acids. We are in flux. And so evolutionarily inappropriate diets of polyunsaturated fatty acids that are already oxidized and susceptible to further oxidation in the human body are causing major issues for people. And I think that there's mechanistic data that points to the actual problem here. There is evidence that as the membrane of your. Of your mitochondria becomes more highly polyunsaturated, you actually get proton leak.
B
Mm.
A
So the mitochondria is a quite a complex little organelle. Right?
B
Right.
A
Probably evidence of endosymbiosis. This primordial connection that we had with some sort of a. A bacteria hundreds of millions of years ago, where a, A, you know, a nucleated organism actually engulfed a bacteria and that bacteria started working for us. And now we have trillions of these mitochondria in our bodies. And this is the way that. Yeah, this is the way that our. This is the way that our bodies convert food energy into kinetic energy. It's through the mitochondria. This is where beta oxidation and glycolysis. Glycolysis happen, or the downstream effects of the downstream biochemistry after glycolysis happen in the mitochondria. So this is where the Krebs cycle happens. And so in order to convert food energy, which is potential energy, to kinetic energy, actual usable ATP, which we use to repair DNA, to make hormones, to make cellular processes, to rebuild our bodies, to run our brains, everything in our body happens with kinetic energy, ATP that comes from food. But in between are our mitochondria. So potential energy and food kinetic energy used to make a vital, fertile, happy, healthy human being. In between is our mitochondria.
B
Right.
A
If you break the mitochondria, and you've spoken about this at length.
B
Yes.
A
If you break the mitochondria, you get stuck with potential energy. And what does that look like. That looks like fat humans.
B
Yeah, yeah.
A
And so it's not. It's not just about calories. Fat insulin resistant humans, it's not just about calories. It's about what are those calories doing to your cellular energy factories. If they are breaking your mitochondria, you are going to store more of those calories. So when you look at a label on Doritos and it says 200 calories per serving, that is baloney, because you can't actually make that Dorito into 200 calories of kinetic energy because there are ingredients in that Dorito, all sorts of ingredients that are breaking your mitochondria. And so when you stuff your mitochondrial membranes, right, there's two mitochondrial membranes. The inner mitochondrial membrane is kind of the ground zero. Inside the mitochondria is where the Krebs cycle happens in deep there. And as you are doing this electron transport chain, you are moving protons across those membranes to create a gradient, and then the protons moving down the gradient through the little ATP motor complex 5 of the mitochondrial electron transport chain. That's what makes ATP. But if those, if those protons are leaking back across, you're not making ATP. And that happens when you stuff your mitochondria with polyunsaturated fatty acids at an evolutionarily inappropriate level. So there's lots of mechanisms by which stuffing your cells full of polyunsaturated fats creates a lot of problems for humans at this formation of energy level. And I think that's what's hard for people to wrap their head around, because it's like, this is mechanistic research and we don't have a study in humans to prove that, because who would fund it?
B
Right, right, right.
A
It's so tricky. But I think that it's pretty clear that we are doing something very wrong as humans today. It's not just that we are eating too many calories, we're eating slightly more calories. But, and I talk about this in the federalye documentary, in the last 20 to 30 years in the United States, we have not increased calorie consumption at all. And obesity has gone from 30% to 42%. We're not eating more calories, we're just getting fatter. What's going on? We're not converting the food energy to kinetic energy because we're breaking our mitochondria. And there are other things that I believe break mitochondria, but I think seed oils are a major factor. We've never had these in our diets. At this level. And I think that the, the way out which you want to talk about is stopping eating so many polyunsaturated fats, particularly this Omega 6.
B
It makes so sense with the big data because, you know, you would think with the parabolic rise in statins.
A
Right.
B
You would have a parabolic reduction in cardiovascular disease, still the number one killer worldwide. We don't see much of a reduction at all in cardiovascular disease, despite the, you know, the revolution of.
A
Right.
B
Of statin. So we are well capable of controlling cholesterol, but we're not capable of controlling the cardiovascular disease. So is it possible. This is just why I want to open people's minds because, you know, your primary care physician might, you know, staunchly disagree with this. Is it possible that we've been actually firing the magic bullet at the wrong target?
A
Absolutely.
B
You know, I, I think that we have. You want to talk about a pandemic? I think we have a pandemic in this country of holding organs responsible for crimes they didn't commit. We do this with the thyroid, we do this with the heart. We do this with the, you know, most people that have, you know, cardiovascular diagnoses of, let's say, hypertension, you know, essential hypertension, or, or, or, you know, type, type 2 hypertension, whatever you want to call it. These people that have essential hypertension, 85% of the time, their, their origin is idiopathic, meaning it's of unknown origin. And so when we don't know the origin, how do we know the organization to hold response?
A
Right.
B
It always fascinates me when we say things like, well, you got high blood pressure. We don't know why, but we're going to medicate the heart. Well, what did you find wrong with the heart? Nothing. So why are we medicating the heart? Well, because we don't, we don't have anything else to do. But if you don't know the, the origin, how do we, how do we go after the organ?
A
Right.
B
And so I think that, you know, I've, I've been deep down the rabbit hole of this lately, and it's, I think the, you know, most of the answers to human physiology are a little more complex and a lot less linear than I think modern medicine likes to make them. Right. We're an ecosystem. Human beings thrive in communities. Our cells thrive in communities. Very often what we do is we take cells out of the body, we study them in a petri dish, we look how they behave in a lab or in certain media that manipulated media, and then we Assume that when we put that cell back into the human body, it's going to behave the same way. And it doesn't because you have this giant community, right? And I think what you're talking about is the, the cause and effect, you know, like the downstream effect of highly processed foods, highly refined sugars, and then all of the direct insults, forget the hormone disruptors and everything that we're putting our skin, but the fake food dyes, the pesticides, the herbicides, the insecticides, the preservatives, all of these things are, are entering this community in our cellular biology and they are wreaking havoc on its capacity to communicate and exchange with its outside environment. It's clogging up our proton pumps. It's actually interrupting our cell walls and our cell membranes. And when you do this at such a, a microscopic level, because we're just a, you know, a thriving community of these organisms, you get these macroscopic results and then we oversimplify it by saying it's just, it's just one thing, right? And so anyway, I, I digress a little bit. But, but so, so let's go back. We put these in. They're, they're pro inflammatory. And in your, your, your case, what you mean by pro inflammatory is they can actually embed themselves into the cell membrane, which is, which is a lipid bilayer by the way. For, for the folks that are, are, you know, what's around your cells is something called a phospholipid bilayer, which a little, a little ring of fat, if you will. And, and not all fat is created equal. And when these, these highly oxidized fats get into those cell membranes, they have a hard time getting out. And that cell membrane is super important because it's the gateway from the interior to the exterior. You know, all of the good stuff is out in the serum of your blood. We got to bring it in. Sometimes there's waste. And by waste, I mean cellular waste. That's got to get out. And if you interrupt these channels now you have a metabolically unhealthy cell. And we know, for example, that all cancer is a metabolic shift in, in the cell, right?
A
It's all connected.
B
It's also connected.
A
It's all connected.
B
It's also connected. Guys, let me let you in on one of my favorite snack foods. This is Masa chips. If you actually look at the back of the ingredients here, you'll see things that you read and pronounce and understand. Non GMO corn, organic beef, grass fed tallow and sea salt that's it. Sea salt, beef tallow and organic non GMO corn. Those are the kinds of ingredients we should be using to fuel our body. Those are whole foods in their natural state. I love these. They come in four or five flavors. These are great for your kids. You can replace your Doritos and your other seed oil laden chips with these. They're not super high in sodium, but they do use a little Redmond sea salt. It's mineral rich. And you know how much I talk about minerals and the need for the body to actually have the 91 essential minerals. We can get these from natural salts. So imagine combining natural salts with organic grass fed beef tallow and non GMO corn. This is a perfect snack. This is guilt free eating. You can replace Doritos. You can actually make nachos with these. All guilt free. Feed these to your kids. I keep them on my shelf. Keep them around. It'll become your favorite snack. Now let's get back to the ultimate human podcast.
A
So linoleic acid, this 18 carbon polyunsaturated omega 6 fatty acid is also the most abundant fatty acid in your ldl. So your LDL is a balloon that carries cholesterol and triglycerides. The most abundant fatty acid in there is linoleic acid. So even if that linoleic acid is not oxidized before it gets in the ldl, the population of the membrane of the LDL changes when you eat more seed oils. So you make a membrane that is more susceptible to oxidation and you make a membrane that is more difficult for your body to manage in terms of oxidative stress at the level of the ldl. So your actual LDL particle is full of linoleic acid when you're eating french fries and cookies and cakes and crackers and dressings. And if you don't eat those things, your LDL remodels very quickly. So let's talk about how to. How to detox.
B
Yeah, yeah, let's talk about that.
A
This is really interesting to me because it connects. It starts to connect a lot of the dots. So canonical thinking is four years. So, okay, that's a long time. But if someone is listening to this and you are eating seed oils and you just stop today, right? Today is the day before Thanksgiving, 2024. If you stop eating seed oils today.
B
We'Ll give you till today after things.
A
Yeah, okay. We'll get one more day.
B
Don't kill them right before Thanksgiving. All right.
A
They have to. Thanks.
B
Okay. Black Friday. Black Friday.
A
Seed oil.
B
Black Friday.
A
You're not Eating seed oils and anything else for the rest of your, you know, next four years, you will almost essentially remodel all of your cells, all the fatty tissues, all of your mitochondria in four years. But there are ways to speed it up and there are things to do to protect your body against the oxidation of these seed oils. Let's talk about speeding it up. This is interesting and probably, I will say from the outset, maybe not super practical for most people. So there are studies in monkeys, sebus monkeys, and I saw this today where they were able to speed up the remodeling from four years to 30 days. Wow. But they fed the monkeys a very, very low fat diet. And when you feed a very low fat diet as a human, you don't feel good. Right. And I'm not really advocating for this. I'm just telling you, research shows this in monkeys. And then it remained. It reminded me of something called the rice diet. You ever heard of Walter Kempner? This guy's fascinating. He died in the 90s, but in the 1950s and 1960s, he took diabetics and he gave them a diet of processed white sugar and rice, a 2000 calorie, very low fat diet of almost white rice and white sugar. And their diabetes got better. It reversed.
B
Wow.
A
But in order to do this, he had to lock them in a hospital. Right. And there's controversy because apparently he had to like whip them to get them, that you cannot keep a human on this diet. I'm not advocating for humans being whipped in metabolic wars, but it's an interesting study that would never be repeated today. Right, right. So it's a very. It's an example of a very low fat diet in humans. And the pictures in his studies are remarkable. It's like a very rotund man and he's rail thin after six months.
B
Really?
A
And the diabetes completely reverses. And even when Walter reversed or liberalized their diet, the diabetes did not come back. So there are now multiple data points of very low fat diets leading to resolution of metabolic dysfunction. And I think what's going on here is accelerated membrane remodeling. Right. So I'm just saying there are ways to do this. It's not easy. If a human wanted to accelerate the remodeling of your membranes, you could potentially eat a lower fat diet for 30, 60, 90 days. Understanding that a low fat diet is not super sustainable for humans.
B
Right.
A
But the other thing you could do is eat a very low polyunsaturated fat diet. You can look at the amount of linoleic acid in your diet and lower it even after avoiding seed oils, should you avoid olive oil? Olive oil can be 12 to 28, linoleic acid. Right. Avocado oil can be 20 linoleic acid. So I think you could accelerate the turnover of your membranes toward a lower linoleic acid membrane state by eating no olive oil, no avocado oil. Again, do it after Thanksgiving. Right. And just lowering the amount of linoleic acid in your diet. Beef tallow, 1 to 2% linoleic acid. Butter, 1 to 2% linolei acid. Avocado oil, olive oil, 12 to 25.
B
Right.
A
Canola 25 linoleic acid. Soybean oil, 50%. Right.
B
Wow.
A
Corn oil, 45% grapeseed oil, 55 to 60% linoleic acid. So if you focus on the low linoleic acid animal fats, the ones we've been told that are bad for us, you can accelerate the turnover of linoleic acid in your cell membranes. And butter especially, I believe could be protective. And I'll tell you why. This is the second piece of this equation. So lower fat oils or fats, animal fats that are much lower in linoleic acid, I believe this will accelerate the turnover of your membranes. There's a fatty acid we were talking about this last night called C15 pentadecanoic acidoic acid. Most of the fatty acids in your cells are odd chain saturated fats. C12, C14, C16, C18, Lauric, Myristic, Palmitic and stearic acid. They're all ODD chain. They're all even chain fatty acids. Right. Odd chain fatty acids, C15 and C17 are starting to be understood, or we're looking at research. And there's research that suggests that C15 levels in your cell membranes can be protective against oxidative stress in your membrane. So polyunsaturated fatty acid peroxidation, lipid peroxidation induced cell death is called ferroptosis. Apoptosis is programmed cell death, but ferroptosis is oxidative stress induced Cell death and C15 levels in your cell membranes protect against ferroptosis.
B
Wow.
A
So the ideal level of C15 in the study that I think was published in 2024, I think it's by Ven Watson is the main author, was 0.4 to 0.64% of your cell membrane is C15. Where do you get C15 in your diet? Butter and rod butter and dairy. Dairy fats and butter are good sources of C15. In fact, they track so much that you can look at someone's C15 levels and tell how much dairy fat they're eating.
B
Really?
A
Again, Dairy fat being something that's been vilified. But you and I had raw milk. And in fact, fact, this. I have to tell the story. So we got raw milk from Southwest Ranches. I love these guys here. They gave us glass containers of raw milk. And this is raw milk from a cow. And this raw milk is so good that you can see the cream on top of the raw milk in the fridge.
B
And I came out to dinner last night and as soon as he left, I slowly poured the cream off the top.
A
You stole the cream off my milk?
B
I literally did.
A
He admitted to it.
B
When he came back, he was like, damn, you don't.
A
Oh, he took, he took all the good cream. But this is such good raw milk.
B
It's a price to stay at my house.
A
I will willingly pay the tax. Thank you for having me at your house. Yeah, but you can see. And we'll post a. I'll post a. On my stories or something. We can post a video together showing this. Cuz I want to show this because there's a lot of raw milk that I get that you can't see. This cream versus milk. But like that cream on top of the raw milk, what you did there, Gary, is you got a C15 infusion by stealing. By stealing the cream off of the raw milk, which I willingly give to you. Happy, happy Thanksgiving. You had C15.
B
Yeah.
A
And that C15 changes the composition of your cell membranes. And that looks to be protective against ferroptosis, lipid peroxide induced cell death. So what are we worried about? What are we worried about with polyunsaturated fats? We're worried about lipid peroxidation, we're worried about cellular damage. Eat dairy fat. This means butter is healthy. Cereals are garbage. So doing more butter and less or no seed oils could also be protective. So in summary, I think there are human and monkey or primate studies showing that low fat diets can accelerate this. And I think if you really want to accelerate turnover of your cell membranes to detox from seed oils, you have to get low linoleic acid in your diet, which probably means even avoiding. If you really want to optimize avoiding avocado oil, avoiding olive oil and focusing on butter, especially with C15 or tallow, long term, that would be. I think that there's a case to be made for that in the research. And look, maybe in this administration we'll actually get some funding to do that study. Right. So this, this is the thing. I will freely say there is no randomized, double blind, controlled trial to prove that. But I'm connecting the dots with the research that's out there. There are mechanistic studies, there are studies to suggest that this happens in both humans and in primates. And so I think it's very reasonable to do that.
B
And you know, what I find is that a lot of randomized clinical trials essentially end up proving what we know ancestrally from nature. You know, it always takes us back to the basics. It's interesting how it comes full circle. You know, we, we go deep down into isolating the oils and, and, and their origin and, and whether or not they're processed or not. And it just basically gravitates us back towards the basic whole food, simple things. Yeah.
A
Like, how can you go wrong eating?
B
Because nature designs it perfect.
A
How can we go. You can't go wrong eating simple whole foods. Whether it's just unprocessed animal foods, unprocessed plant foods, you'll be great.
B
Yeah. So I want to go down the road of supplementation, right? I mean, we have essential fatty acids, we have essential amino acids, you know, essential, meaning they're necessary for life. I don't think many people are, are not getting these, but there's so many different fatty acid supplements. Fish oil supplements, black seed oil supplements. I know plenty of people that do a shot of really good olive oil first thing in the morning, which, which I'm actually a fan of. I need, I need enough of it that I don't have to do it. But I'm a fan of people that don't get enough doing that. So what are, you know, first of all, can you, can you, can you give a little explanation of the difference between an omega 3 fatty acid and an omega 6 fatty acid and why the ratio is important?
A
Yeah.
B
And where we get omega threes and six. And, you know, if somebody's listening to this and they want to start taking a BPA or DHEA or needs to take a fatty acid supplement, right. You know, what do you recommend? Or you do recommend getting it for diet.
A
So Omega 3 is also polyunsaturated, and Omega 3 versus Omega 6 is just a nomenclature designation based upon where the first double bond is based from the end of the molecule. So if you look at a fatty acid, it's a long chain of carbons with a carboxylic acid group on the end and the first desaturation point, which is a double bond if it's close to the end of the molecule, if it's three carbons from the end, we call it an omega 6. Omega 3. If it's six carbons from the end, we Call it an omega 6. Right. Omega 3s are in much smaller amounts in our diets than omega 6s and.
B
Need to be in higher amounts.
A
Yeah, well, they probably should be in higher amounts for most of us. Right. Many of us, you and I get plenty of omega 3s and maybe don't need to increase. Right, right. Omega 3s occur naturally, and omega 3s, we're talking about ala, which is alpha linolenic acid, not linoleic, Alpha linolenic acid, DHA, do casa, hexaenoic acid, epa, icosa or ecosa, hexa or ecosapentanoic acid, and DPA do casa, pentanoic acid. And there's a, there's a sort of a biosynthesis pathway and the pathways parallel. Right. So the, there's the same exact series of enzymes. These are desaturases and elongases that turn ALA into dpa, and they also turn linoleic acid into arachidonic acid and other omega 6 downstream metabolites, plates. And so D5D, D6D. These are shared enzymes between omega 3 and omega 6. And one of the things we know is that if you're eating a lot of Omega 6, and I would argue that humans are eating evolutionarily inappropriately high amounts of omega 6 and probably for many evolutionarily inappropriately low amounts of omega 3, because processed foods don't have much omega 3, but they're full of omega 6. This is a problem because these parallels are path are these, these pathways are parallel. And when you eat two micromega six, all the enzymatic activity of those shared enzymes goes to the omega 6 pathway. You can't really biotransform the omega 3s. Right. You can get preformed omega 3s in your diet, but you are not really going to be able to biotransform anything that you're. If you're getting ALA, alpha linolenic acid or any of the upstream omega 3 metabolites and you want to turn them into DPA or downstream metabolites, you can't do that. Well if you're eating a lot of omega 6. So if you look at the amount of omega 3 that I eat, it's pretty small in my diet, relatively speaking. I have egg yolks sometimes and I get my omega 3s from animal fats. There's omega 3s in that cream on the milk. Right. There's omega 3s in meat. I don't feel like I need to supplement with a fish oil because I'm eating unprocessed animal foods that are primarily fed grass. And my body can biotransform alpha linolenic acid into epa, dha, dpa. I've done these checks and I have lots of epa, DHA, and DPA in my body. And I don't take a fish oil supplement.
B
Good.
A
Because I'm eating less omega 6. I don't have very low levels of omega 6, so my body can use those parallel enzymes.
B
Omega 6 come from.
A
From the omega 6 comes from seed oils, right? Primarily, yeah. You can get a little bit of omega 6 if you're eating almonds. I don't think that's a problem for most people if you can digest almonds. That's a separate conversation that we've had about, I don't think almonds are very digestible. But you're not. You're not getting a lot of omega 6 if you're eating unprocessed plant foods. You're just not. But you're getting a lot of Omega 6 from the seed oils. Now, asterisk, we are also getting evolutionarily inappropriate amounts of omega 6 from things like chicken and pork. Because going back to our previous point, humans, chickens and pigs are all monogastric animals. We all store polyunsaturated fats. When you are eating a chicken, and the chicken thigh is going to be fattier. If you're eating a chicken thigh, and that chicken is fed corn and soy, just like humans that are fed corn and soy oils, that chicken is accumulating linoleic acid in their fatty acid in their tissues. So chickens, historically, if you look at wild chickens, 4% linoleic acid in their fat. Chickens today, 20%.
B
Wow.
A
Same with pigs, 4 to 5%. Wild hogs. Right. 4 to 5% linoleic acid in their tissues today, 20% linoleic acid in the tissue. So do I think that eating traditionally raised pork and chicken is the major contributor to. No, this is not the biggest. It's mostly seed oils.
B
Right.
A
But if somebody is really trying to be aware of evolutionarily appropriate, biologically appropriate consumption of linoleic acid, you have to start thinking about your bacon. I'm sorry. And look like you can do it, you know, raise your own pigs, let them root in the ground, let them eat bugs and worms and mice, because they do eat other animals, and let them eat roots. Don't feed Them corn and soy, and your pigs will have much lower amounts of linoleic acid. There are more and more of these producers out there doing low la pork.
B
Wow.
A
Historically, we are eating pork that is full of linoleic acid because of what they're fed. So most of it is coming from seed oils, and it's coming from. And this also happens with our eggs. Gary, too, which is why it's important to eat chickens or eggs from chickens that are eating the right things. Right, Right. So if chickens are eating better, there's less linoleic acid in their eggs. But if chickens are eating corn and soy, they pour more linoleic acid into their eggs. And so there was recently an article that came out about this. You know, like, the amount of linoleic acid in egg yolks is higher than it probably should be historically.
B
Wow.
A
So the quality of what your chickens is eating. And I don't want this. At this point, I'll pause and say, I don't want this to be overwhelming for people.
B
Right.
A
Knowledge is power. Know better, do better.
B
Right.
A
I'm just offering information that anyone listening to this can use wherever they are on their health journey.
B
Right.
A
If your first step is getting rid of seed oils. Get rid of seed oils.
B
Yeah.
A
Keep eating pork, keep eating chicken, keep eating your eggs. Don't worry about that yet. That's step three. That's step three. But I'm giving you all the steps. Right, Right. So that's where all of the linoleic acid is coming from in our diets. And it's kind of. It's kind of tough because when you think about it, we're getting it from all angles. If.
B
Yeah.
A
If the chickens that you're eating are fed corn and soy and the pork you're eating is fed corn and soy, and the eggs are coming from chickens that are fed corn and soy, and you're eating sweet oils, and then you're making.
B
And you're making sauces, you know, out of corn and soy.
A
Yeah, yeah. Then how is it any wonder? You know, like, think about all of these inputs in our diets and this. I'll go back to this phrase, evolutionarily inappropriate consumption of excess amounts of linoleic acid in our diet. And I think it's a real problem for humans. And again, it happens at every level. The good news here is that beef is a ruminant. Right. Beef. So cows, bison, lamb, elk, deer, these animals do not bioaccumulate linoleic acid. They have the biochemical machinery to saturate polyunsaturated fatty acids. We do not. So if a cow is fed grains, it has essentially the same amount of linoleic acid in its fat as a cow that's fed grass. I think a cow is better when it's fed grass. But a grain fed cow does not have the same magnification of linoleic acid in its tissue as a chicken. As a chicken or a pig. Because they're monogastric or a human. Right. We're eating humans, but like humans store this. So we have the same issue. There's evidence from I guess archaeology or anthropology that in our fatty tissues humans historically had 2, 3% linoleic acid and now we're looking at 20 plus percent.
B
Wow.
A
Linoleic acid or fat. So we are the same as a chicken or a pig.
B
And what's the consequences of all of this linoleic acid? Is it because it its composition of the the cell membrane?
A
Back to the mitochondrial thing we talked about with a proton leak and you know, potentially impairing at a cellular energy level. The hypothesis which I think is supported by the literature is that it's impairing the biotransformation of potential energy to kinetic energy.
B
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A
I'm not advocating for that.
B
That one really caught me off guard.
A
But it's low fat. It illustrates the point, right?
B
Yeah, yeah, it's low fat, illustrates the point you use. You actually see it's like the tide raises and lowers all the ship. You see, you see like increase, you know, the thyroid production of T4 starts to rise, C reactive protein goes down, homocysteine levels drop, filtration rates increase. In the kidneys. You See obviously Hemoglobin A1C 3 month averages of blood sugar going down, fasting insulin reducing over overall insulin levels, reducing even alkaline phosphatase and, and liver enzyme levels, ast, gdt, you know, alt, these, these, these sort of secondary markers of inflammation in the liver, you know, and and not that all these levels collapse, but if you, if you compare labs 10 weeks apart and all you did was really put them on something like a carnivore diet or in some cases a keto reset, you see this systemic improvement in all of these levels. And you know, that's, that's probably a podcast for another time. You know, the gut being the gateway to the rest of the body. But I, I have seen those, you know, those, those results super powerful too. And a lot of it is, you know, probably eliminating these seed oils, but the, the positive effects are rather immediate.
A
I mean, you know, I mean, you and I both, I mean, I, we talked about this on the first podcast that we did. I wrote a book about the carnivore diet.
B
Yeah.
A
I think that something with more foods works better for me and a lot of people long term. But, but think about what happens if you just eat steak. You are just eating animal fat, which is very low in linoleic acid. You're essentially doing a gut reset because you're just eating meat, which is very highly digestible for most people, contrary to popular belief. And you're eating only animal fat. You're not eating olive oil or avocado oil, you're not eating any seed oils, you're not eating any oils that are high in linoleic acid. A lot of things get better. I think that for a lot of people, it doesn't work long term. It gets a little too limiting. Right.
B
That's why I said 10 weeks.
A
Yeah, yeah. But it can be really powerful. And I think that this is where I'm interested in this idea of an animal based stuff diet kind of this in between. And on some recent podcasts, I thought maybe animal based is kind of like carnivore 2.0. Right? You do, maybe you do carnivore as a reset or you can just go right to animal based and animal based for people that don't know. It's just a term that I, that I've used to help people understand the framework is like meat plus fruit.
B
Right.
A
So like, you know, I've got some squash in there on the table. Squash is a fruit.
B
You're making orange juice in the ring.
A
Making orange juice. Like, but the meat plus the fruit and obviously you're getting the organs in there too. That's, that works really well as well and is a little more sustainable.
B
And you're not afraid of the, you know, the fructose, fructose in the, in the blueberries. And it's, it's really the Combination of having the glucose and the fructose together, I think the body's metabolizing those, not just the presence of fructose on its own.
A
We, I think we talked about a.
B
Lot of people attack blueberries, and it's crazy.
A
And. And I've even seen people attacking honey.
B
Yeah.
A
And you and I, we. We geek out on honey because I brought you this honey from my house in Costa Rica. Mariola honey, dude.
B
Oh, these are bummed that you didn't bring it to stingless bees.
A
I'm bringing it next time.
B
Stingless bees. Those are my kind of bees.
A
They're amazing. So I have a hive in my house. Mariola honey. But there's been people attacking honey recently. But if you look at the medical literature, you can't attack honey.
B
Yeah.
A
I mean, honey improves insulin sensitivity. Sucrose, not so much, which is, you know, this pure molecule that's been extracted from the honey. Honey has over 300 bioactive compounds.
B
Yeah.
A
But honey improves metabolic function in humans, and honey improves testosterone. And there's review papers written about honey for metabolic illness. It's wild. And we get so myopic in medicine, kind of like with the ldl, we just focus on blood glucose.
B
Right.
A
Blood glucose is a symptom of underlying metabolic dysfunction. It's not the metabolic dysfunction.
B
Right.
A
Eating honey does not cause insulin resistance. Honey doesn't cause diabetes. If you have diabetes, honey is going to spike your blood sugar, but it didn't cause it. Right. So if you have diabetes. Yeah, don't eat as much honey as you or I. But small amounts of honey, probably beneficial, and honey didn't cause the problem. We have to point. We have to point the weapons at the actual cause.
B
Right.
A
If you point the weapon at the wrong cause, you're just putting your resources where they shouldn't be. And as we talked about, apob. Wrong place to put your weapon.
B
Right.
A
Insulin resistance, glucose, fructose, Wrong place to point your weapon. Point your weapon at insulin resistance.
B
Right.
A
The same thing with fruit. If you look at someone who's trying to make a case that fructose is harmful, invariably they will cite studies in animals who don't have the same biochemistry. They do much higher rates of de novo lipogenesis when they presented with fructose. Meaning if you give fructose to a rat, it's making much more of that into body fat than when we do as a human, we do 1%. You give a human 1% of fructose goes to fat via de nova lipogenesis. Most of it goes to glucose, it goes to, you know, glycogen, it goes to lactate, like, like glucose. I mean, fructose doesn't turn into fat in humans anywhere near like it does in animals. So you can't look at animal studies for fructose metabolism because it's completely different. Right? It's completely different. And if you look at human studies with fructose, they are, as you suggest, invariably giving pure fructose. There's not a single fruit or honey or anything on the planet where you're getting pure fructose without glucose.
B
Right.
A
And in the gut it's all sim porters, it's all transporters that need glucose and fructose to move across the gut lining.
B
Yeah.
A
And so if you get free fructose in the gut, it gets stuck in the gut. Well, what happens if fructose gets stuck in the gut? It causes overgrowth of pathogenic bacteria.
B
Right.
A
And then you get, you get, you get lipopolysaccharide, you get endotoxin. So they've done these studies in animals where they'll give free fructose and they'll give something that blocks TLR 4 or 5 toll like receptor 4 or 5, which is what endotoxin triggers eventually. And the negative effects of fructose are essentially abolished.
B
Wow.
A
So the negative effects of fructose at the level of the gut and humans is driven by endotoxin. And we don't get more endotoxin when we eat fruit. In fact, I think you could easily make a case that when you eat a blueberry or you're eating a persimmon or you're eating orange juice and a toxin which is lipopolysaccharide goes down. But the harmful effects of fructose in humans are isolated fructose feeding leading to lps. So it's just, it's, again, it really mirrors a lot of the discussion around seed oil research or apob. I think that the people, I think that people in the health space are well intentioned and super intelligent. But I really hope we can all come together and consider all of the research in its entirety with candid, with candor, you know, because I think that if you just, if we're, it's hard, we need a lot of people to look at this because it's easy for one person and, and I will raise my hand, you know, like, I want to collaborate with people who think differently than me. It's easy for one person just to see the research in less than its entirety. And if you're only Looking at the fructose research in humans that's isolated fructose feeding, or you're only looking at the research with LDL in people that are insulin resistant, or you're only looking at the seed oil research in the trials that are flawed because of their design.
B
Right.
A
You're going to come to the wrong conclusion.
B
Yeah.
A
And that's the problem here.
B
Yeah, I totally agree. Well, what else is exciting you, man? What's, what's, what's new with Paul Saladino, man?
A
I think that like all of this is super exciting for me.
B
I mean, I mean, I mean the ability to affect public policy research, we talk about this all the time, is, you know, maybe to be Maha. Yeah.
A
Make America Healthy again gets me pretty excited. Yeah. I was pretty bummed to see RFK Jr. With the photo of the McDonald's.
B
Come on.
A
But I believe, I believe his heart is good and I'm really excited to see where it goes over the next four years. I mean, who. Jay Bhattacharya? Did you see this head of the nih? Yeah, this researcher from Stanford was recently nominated for the head of the head of the nih. So Jay Bhattacharya was one of the guys kind of raising the alarm during COVID Oh, yeah, yeah.
B
No, no, I did receive it. He was appointed.
A
Yeah, he was, he was nominated for the head of the NIH, you know, RFK Jr. Head of Health and Human Services. I think Marty McQuarrie is head of the FDA potentially.
B
Right.
A
So it's going to be interesting to see where this goes.
B
Yeah.
A
Because I think that at the level of the Senate, you have a Republican controlled Senate, but you have a lot of people in the Senate who have ties to big food. So I think that there's going to be an. Hopefully there's enough pressure.
B
Five lobbyists, according to Cali Means. I mean, five lobbyists for every member of Congress.
A
This is crazy.
B
That's my number.
A
It's mind blowing.
B
Humanity is just five people whose 40 hour work week is designed to do nothing but influence your decision, decision making. I mean, and the, the amount of inbound that you must have to deal with. Just, just, you know, five people assigned just to you for a single sector of what you're working on as a, as, as a congressional service person. I mean, it's pretty, pretty intense. And I think there's a lot of light being shed on this now. The corruption, the food supply corruption and nutritional research, you know, the, the conflicts of interest, you know, they talked about.
A
Worse at the usda. So Maybe, Maybe somebody was. I mean, there's. I wonder who's going to head the usda. But Nina Teicholz, who's in this seed oil documentary, has pointed out 19 out of 20 members of the USDA Dietary Guidelines Committee, 2020-2025 had ties to pharma and processed food industry. Things like ilsi, the International Life Sciences Institute, which is just a euphemistic title for a lobbying group for Pepsi and Kraft and General Mills. 95 of them had ties. This is the USDA Dietary Guidelines Committee that makes policy for food and food stamps and school lunches. Yeah, it's crazy.
B
It is.
A
It's really, absolutely ludicrous. The amount of corruption at those levels is sickening.
B
Yeah. And look, the amount of damage that the corruption caused is really what's sickening. I mean, you know, I think politicians have been taking, you know, money for favors for, for decades. But, you know, this is especially troublesome, you know, especially in the era where we have the highest rates of childhood cancer that we've ever had, had highest rates of childhood obesity that we've ever had. The, the most skyrocketing rates of autism, Asperger's, add, adhd, ocd, manic depression, bipolar. Like these conditions that you just never heard of 30 or 40 years ago, 50 years ago that are now so prevalent. You know, I, I remember RFK made a statement. It really hit me, hit home with me. He said, when I graduated high school and I graduated high school in 1988, something really dating myself there. You know, I just, I didn't know an autistic child. I didn't have any autistic friends. I didn't know what that was. And I didn't know someone who knew someone who was. My 16 year old, knows 10 kids in her school. She could name 10 people that openly, you know, have autism or they're in, in, in programs that are related to, you know, autistic children or, or kids with other kinds of neuroinflammatory conditions. And you think, wow. But, you know, that. Super anecdotal, but, you know, in my mind, it went from 0 to 1 and, you know, to, to 10.
A
And this is not increased screening. This is not, this is increased incidents.
B
Right.
A
This is not that we're more aware of it. This.
B
No.
A
When you were in high school. When I was in high school, there were not undiagnosed kids. There was just no kids.
B
Like, Right.
A
When someone has.
B
It wasn't socially, you know, unpopular, you know, like, like.
A
Right.
B
Like some of the Sexual choices today. It wasn't, wasn't that people were hiding it. It was that they just didn't have. You don't exhibit.
A
These are not something you can hide. Yeah. This is increased incidence. This is humans getting less healthy in front of our eyes.
B
Yeah.
A
In the real time.
B
To continue the corruption at that level with that kind of expense.
A
It's crazy.
B
You know, is, is astounding to me. But.
A
And we talked about this earlier, the USDA recently came out and tweeted, we don't have enough data that ultra processed food.
B
I saw that. Ultra processed foods.
A
I was like, what are you doing? The USDA Dietary Guidelines Committee, 2020-2025. Thankfully they're out of here in like a year.
B
Not even a couple months.
A
Yeah, yeah. Okay. So they, they tweeted, we don't have enough data. We need more data. Who's gonna fund it that ultra processed foods are behind the obesity crisis? Are you crazy? I mean, there's. Kevin hall did a study about this and there's another study that was published that' the exact same thing. You put people in a metabolic ward, you control everything they're eating for two weeks. When you give them the same amount of calories, but they can eat as much as they want in ultr processed food or processed food. Ultr processed food or unprocessed food, they consistently eat more ultr processed food. They gain two pounds a week, I think was the study maybe. Yeah, something like that. Two pounds a week unpressed food.
B
Dr. Hyman talked about this.
A
They're given the exact same calories. They try to match everything for sugar, salt, fat, macros.
B
Yeah.
A
The ultra processed food is just more addictive. It doesn't trigger satiety.
B
It's more addictive. And it, and, and it's less, you know, it's nutrient deprived and so it's less satiating. Right. And if you look at the mechanisms for GLP1.
A
Right.
B
You know, they have a lot to do with the nutrient density of food releasing the GLP1 giving us that satiation response. So if you don't release the GLP one, if you don't create a satiation response, you're now just, just you eating the same volume and caloric intake. And you're. And you're still hungry because your brain is like, I still need beta carotene and iron and, and you know, I need a complex of B vitamins, like I'm nutrient deficient. So let's keep putting stuff in so I can just get the basics of, of what I Need. I mean, inherently, we know that there's.
A
Natural, natural ozempic, it's meat and you know, plant foods, like.
B
Yeah, try to overeat rib rice.
A
Yeah, it's hard meat. Try to overeat a steak, you know, like, that's natural ozempic, man. Like meat in a salad. Meat and fruit. It's hard to overeat that, which is why it kind of kills me, you.
B
Know, I think it's so, so crazy that we push down on the top of this pandemic of obesity rather than pushing up from the bottom, you know, I mean, again, it's the toxic soup. We're bathing our cellular biology and not just this magic, you know, obesity sort of. It, you know, I, I, I think, I think classifying it as a disease makes people think it happened to them and not have within them.
A
Yeah.
B
Do you know what I mean? Like, I caught this, like I caught the flu.
A
Right, right.
B
That happens. You know, you got a plane, you took a long flight and then, you know, the next morning you woke up and you got a sore throat or, you know, you're sick. I mean, that, that, that the influenza happened to you. Diabetes didn't happen to you. Right. It happened within you. And I think that if we can sort of shift the narrative a little bit, you know, get physical education back in the public school system.
A
Put them in the sun.
B
Stop. Yeah, put them in the sun.
A
Put kids, they do let them go on recess.
B
But I saw Tim Gray from, from the UK did it, did a post the other day where he actually showed a study that, that prisoners, incarcerated prisoners, get more sunlight on a daily basis than grade school children because they're actually required by law.
A
Oh my God.
B
To be outside for an hour. They're given an hour outside every day. Whereas, you know, kids get in a cover, go from covered house to a covered garage to a covered car to a covered school, staying there all day, and then go to a covered car to a covered garage, back to a covered house. And, and, and, and, and we just, you know, wonder why we're facing a lot of these crises. And, and eventually the research is just going to, again, it's going to bring us back to the basics. Sunlight grounding, you know, movement, exercise, whole foods, and, you know, the, the, the possibility of even cleaning up the public school food. When they made the announcement that, that, you know, the federal government was going to subsidize lunchables for the public school system. This isn't even food.
A
What?
B
Yeah, we're getting way off the, going way down the rabbit hole.
A
But no, but it's all relevant. It's all connected. We're not that far down the rabbit hole. And you've seen this clip of Fatima Stanford, who I think is a Harvard physician on 60 Minutes with Barbara Walters telling her that obesity is a genetic disease. I know, and I will paraphrase her, but I'm basically, this is pretty close to what she said. She said even if you, you do diet and exercise right, 60 to 75% of people will become obese.
B
That is, that is absolutely not. Why didn't we have this in the 50s then?
A
It's malarkey.
B
We had genetics back then. Oh my gosh.
A
And, and she's paid by Ozempic. She's on. And going back to what we were saying earlier, Darius Mozafarian, who writes this meta analysis on seed oils paid by Bungee Seed oil manufacturer. Right. So again, I'm not saying it's all like that. I think they're researchers, get it right, get it wrong, even if they're not funded by industry. But let's be honest about who's funded by industry. And really talk about this when, you know, when your Tufts, you know, nutrition food Compass guy is funded by seed oils.
B
Yeah.
A
He's funded by ultra processed food. And you know, and then this, this woman at Harvard is on 60 Minutes saying it's a genetic disease. You're receiving funding from Ozempic. Come on.
B
Yeah.
A
What are we doing?
B
Tell me, what gene in the genome carries the fat gene?
A
I mean, where's the fat gene?
B
Yeah, yeah. I don't know. I've spent, you know, the balance of my adult lifetime studying epigenetics, and I don't know about that gene, but it's genetic.
A
Genetic, Gary, you can't avoid it.
B
You know, we say it's genetic very often when it runs in families. And a lot of times that's, that's another fallacy is that because things run in families, they're genetic. And that's, that's absolutely, patently false. I mean, there are certainly conditions that are genetically inherited, but significantly less than we've been when led to believe. And one of them is definitely not obesity.
A
I think you can be predisposed, but the predisposition is not a predetermination.
B
You can put somebody without, without the fat gene in, in, in, in the, in the wrong environment.
A
Right.
B
And, and they're going to be obese.
A
Right.
B
Obesity is. And you know, when I, when I would go to Disney World or, or Universal Studios, you know, I Always tell the story of. You know, I spoke at Access Hollywood one time and I was walking from the, the back of the park where they picked me up to the, to the studio. And as we're cruising through the park, you know, I, I mean, you, you want to see what bad shape we're in as middle America. Just, just go to Disney World, right? And just take, take a look around. And I made a comment about the fanny packs that people were wearing and I was like, what's with the fanny pack pandemic? And I was just making a joke because everybody I saw had a fan pack on. And, and the security guard just very flippantly said, oh, that's because they can't put their hands in their pockets. And I was like, whoa, dude, you're right. They actually can't get their hands in their pockets. But, but my, my other point is that you could see the lineage. You know, there was like obese grandma in the motorized wheelchair very often with a 2 liter of soda in the basket.
A
Oh, yeah, yeah.
B
And then, you know, mom is, you know, kind of waddling not far behind, and then rather obese 12, 13 year old kid. And I don't think the grandmother passed the gene to the mother, passed it to the son. I, I think you look at the, you know, the epigenetic.
A
They're all eating the same food, they're all in the same environment.
B
And then he's sitting on a, you know, bench with a, you know, a funnel cake and a 64 ounce Big Gulp. And I'm running the math in my head. I'm like 64 ounces of soda. Okay. So that's 29 tables teaspoons of soda. Okay, so that's because it's five soda sugar. Yeah. Like running the math. And, and a funnel cake is just, just white flour, deep fried and seed oil with 10x sugar.
A
Yeah.
B
And he's just, that's, that's what's going in. I'm just like, you know, and of course he's sniffling and wiping his face. And I just felt, I felt bad and I felt like how uninformed these people must be. Because, you know, if you, if you went to that mother, she loves her kid, you know, I consider a child abuse. But that, that also implies that they really are aware and know what they're doing.
A
Right.
B
Just the, the pendulums just swung that far. We're that far off of any assemblance of even basic, you know, fundamental nutrition. So.
A
And I think that RFK Jr put this in the right Context. This is poison. I think that you have foods that promote health in humans and then you have poison.
B
Yeah. And you have non foods and then you have poisons.
A
I agree, I agree. You have poisons.
B
You got like, like, you know, serves you neutral damage. Right.
A
These are metabolic poisons.
B
Yeah, yeah.
A
Metabolic poisons that are legal. So cigarettes regulated, alcohol regulated. Right. Raw milk is illegal in many places, but metabolic poisons are legal and that's what's not. I don't think we've really framed it in that perspective. That, like, I would see this as you go to McDonald's. That is a metabolic toxin. You are actively poisoning yourself. And look, we all do it. I've had alcohol in my life. Alcohol is also a toxin.
B
Right.
A
I. I've smoked one and a half cigarettes in my whole life. There's a whole story about that. Yes, but like we all engage in some toxic. No question, it's part of being human. Eat birthday cake with your kids. But look, if you don't understand that that is a metabolic poison and your body will cross a threshold at. At which point your metasm, your metabolism, your mitochondria will become broken. We're missing the plot.
B
Yeah, I agree.
A
These are poisons.
B
Yeah, I agree. Paul, thank you so much, man. And I'm sorry for stealing your cream.
A
We got more.
B
It's been amazing having you on. You know the last question that I always ask my guests, I asked you this last time, but what does it mean to you to be an ultimate human?
A
And I probably will answer it in the same way. I don't remember exactly how I answered it. For me, it means being able to get up, up, put my bare foot, bare feet on the ground, put the sun in my eyes, hopefully go in the ocean and get some grounding, be in nature and spend time with people I care about in nature and have the health and the vitality that is necessary to do that, like being able. For me, the best part of my life is spending time with people I care about in nature. And I need health and I need vitality to do that. Whether we're surfing, whether we're climbing mountains, whether we are snowboarding in the mountains or whether we are in the ocean, you know, just in a river. Like, that is being the ultimate human. And like my vitality, my energy, my motivation, my strength comes from having a metabolism that works. And so I need. I need to be healthy to be able to do those things and make the memories that I will treasure for my life.
B
Yeah. Amen. Well, that's great. Guys. And as always, that's just science.
Podcast Summary: Episode 129 – Paul Saladino, MD: Why 'Heart-Healthy' Seed Oils Are Actually Poison
Introduction
In episode 129 of The Ultimate Human, host Gary Brecka engages in an in-depth conversation with Dr. Paul Saladino, a prominent Human Biologist and longevity expert. Together, they explore the hidden dangers of seed oils, challenging mainstream nutritional beliefs and delving into the biochemical impacts of these commonly used oils on human health.
Overview of the "Fed a Lie" Documentary
Paul Saladino introduces his documentary, "Fed a Lie," developed in collaboration with Heart and Soil Supplements. This 37-minute mini-documentary aims to unveil the inflammatory nature of seed oils and their suppressed negative implications in numerous chronic diseases. Saladino highlights contributors like Dr. Chris Kenobi and Nina Teicholtz, author of The Big Fat Surprise, who discuss the purported corruption and confusion within the nutritional food industry.
Notable Quote:
Paul Saladino [03:58]: "Those are testicle pills from Heart and Soil supplements. And Heart and Soil is just a company that I built to tell people to get organs in the capsules."
The Harmful Effects of Seed Oils
Saladino meticulously dissects the composition and processing of seed oils—such as canola, soybean, sunflower, and corn oil. He explains that these oils undergo extensive refining processes, including grinding, heating to temperatures exceeding 500°F, bleaching, and deodorization. This treatment leads to the formation of lipid peroxides, making seed oils highly susceptible to oxidation.
Notable Quotes:
Paul Saladino [09:24]: "When you heat linoleic acid to 500 degrees Fahrenheit, you get massive amounts of lipid peroxides, which is essentially rusted oil or rancid oxidized oil."
Gary Brecka [14:19]: "We are stuffing our cell membranes and our mitochondrial membranes with polyunsaturated fatty acids."
Saladino emphasizes that the consumption of these oxidized oils fosters inflammation, evidenced by increased markers like oxidized LDL and LPPLA2. He critiques the mainstream medical community, including institutions like Harvard and Mayo Clinic, for maintaining the misconception that seed oils are harmless despite mounting evidence to the contrary.
LDL Cholesterol and Atherosclerosis
The discussion shifts to LDL cholesterol, where Saladino challenges the traditional view of LDL as inherently atherogenic. He uses anatomical examples to illustrate his point, noting that while LDL circulates in both arteries and veins, atherosclerosis predominantly affects arteries due to factors like higher pressure and resultant endothelial damage.
Notable Quotes:
Paul Saladino [23:46]: "If APOB is what we should be lowering without any attention to insulin sensitivity, oxidized LDL, LPPLA2 is just ludicrous to me."
Gary Brecka [21:35]: "If you have a lot of dry wood in your body, the dry wood being the oxidation susceptible linoleic acid, and you have lots of sparks, you're going to get lots of fires and then you're going to overwhelm your body's resources."
Saladino posits that insulin resistance, rather than LDL itself, impairs the immune system's ability to repair arterial damage, thereby promoting atherosclerosis.
Diet, Mitochondrial Health, and Membrane Remodeling
A significant portion of the conversation delves into how dietary polyunsaturated fats, particularly linoleic acid from seed oils, disrupt cellular and mitochondrial membranes. Saladino explains that excessive intake of linoleic acid leads to proton leaks in mitochondria, impairing ATP production and energy metabolism.
Notable Quotes:
Paul Saladino [32:57]: "We are stuffing our cell membranes and our mitochondrial membranes with polyunsaturated fatty acids."
To counteract these effects, Saladino recommends adopting low-linoleic diets by eliminating seed oils and favoring animal fats like butter and tallow, which are substantially lower in linoleic acid. He also introduces the role of pentadecanoic acid (C15), found in dairy fats, in protecting cell membranes from lipid peroxidation and ferroptosis—a form of oxidative stress-induced cell death.
Supplementation and Fatty Acid Ratios
The balance between omega-3 and omega-6 fatty acids is highlighted as crucial for maintaining healthy enzymatic activity and reducing inflammation. Saladino advises minimizing omega-6 intake from seed oils and ensuring adequate omega-3 consumption through whole foods rather than supplements.
Notable Quotes:
Paul Saladino [51:05]: "Omega 3 is also polyunsaturated, and Omega 3 versus Omega 6 is just a nomenclature designation based upon where the first double bond is based from the end of the molecule."
Gary Brecka [54:03]: "And the consequences of all of this linoleic acid? Is it because its composition affects the cell membrane?"
He emphasizes that most of us consume excessive omega-6 due to processed foods, which disrupts the biotransformation pathways essential for converting omega-3s into their beneficial forms.
Public Policy and Food Industry Influence
Both Brecka and Saladino express deep concern over the influence of big pharma and the processed food industry on nutritional research and public policy. They criticize the USDA Dietary Guidelines Committee for having most members tied to industry lobbying groups like the International Life Sciences Institute, arguing that this has led to policies favoring processed foods and seed oils.
Notable Quotes:
Gary Brecka [17:46]: "This is ludicrous. This is the state of the affairs right now."
Paul Saladino [56:22]: "The USDA Dietary Guidelines Committee... 19 out of 20 members had ties to pharma and processed food industry."
Societal Outcomes and Modern Diets
The speakers connect the consumption of ultra-processed foods, rich in seed oils, to rising rates of obesity, diabetes, autism, ADHD, and other neuroinflammatory conditions. They cite studies demonstrating that people consuming processed foods tend to gain more weight compared to those eating whole, unprocessed foods, even when calorie intake is controlled. This is attributed to the lack of satiety signals and the addictive nature of processed foods.
Notable Quotes:
Gary Brecka [73:15]: "The USDA Dietary Guidelines Committee... tweeted, we don't have enough data that ultra processed food."
Paul Saladino [74:23]: "There are mechanisms for GLP1... releasing the GLP1 giving us that satiation response."
Conclusion and Final Thoughts
Concluding the episode, both Brecka and Saladino emphasize the importance of adopting whole, unprocessed foods to enhance longevity and overall health. Saladino defines "being an ultimate human" as achieving health and vitality through a metabolism that functions optimally, supported by a diet free from harmful seed oils and rich in nutrients.
Notable Quotes:
Paul Saladino [82:33]: "For me, the best part of my life is spending time with people I care about in nature. And I need health and vitality to do that."
Gary Brecka [81:27]: "We are bathing our cellular biology in this toxic soup and then allowing that to be the answer without actually changing the habitual pattern that brought you there."
Key Takeaways
Disclaimer: The views expressed in this podcast summary are those of the speakers and do not constitute medical advice. Listeners are encouraged to consult with healthcare professionals before making significant changes to their diet or health regimen.
This comprehensive summary encapsulates the critical discussions and insights shared by Gary Brecka and Dr. Paul Saladino, providing listeners with a clear understanding of the potential dangers of seed oils and the importance of whole, unprocessed foods for optimal health.